2024-03-29T08:47:54Zhttps://eprints.lib.hokudai.ac.jp/dspace-oai/requestoai:eprints.lib.hokudai.ac.jp:2115/537262022-11-17T02:08:08Zhdl_2115_20044hdl_2115_124Pyrroloquinoline quinone prevents oxidative stress-induced neuronal death probably through changes in oxidative status of DJ-1.Nunome, KanaMiyazaki, ShinNakano, Masahiko1000090184283Iguchi-Ariga, Sanae1000020143505Ariga, Hiroyoshiopen accessDJ-1pyrroloquinoline quinoneoxidative stressneurotoxityAnimalsAntioxidants/pharmacologyAscorbic Acid/pharmacologyBlotting, WesternCell Death/drug effectsCell Survival/drug effectsDose-Response Relationship, DrugFemaleHydrogen Peroxide/antagonists & inhibitorsHydrogen Peroxide/toxicityMicrotubule-Associated Proteins/drug effectsMicrotubule-Associated Proteins/geneticsMicrotubule-Associated Proteins/metabolismNeurons/drug effectsOxidants/antagonists & inhibitorsOxidants/toxicityOxidation-ReductionOxidative Stress/drug effectsOxidopamine/antagonists & inhibitorsOxidopamine/toxicityPregnancyProtein BindingPyrroles/pharmacologyQuinolines/pharmacologyRatsSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationTetrazolium SaltsThiazolesTumor Cells, CulturedVitamin E/pharmacology499Pyrroloquinoline quinone (PQQ) has been shown to play a role as an anti-oxidant in neuronal cells and prevent neuronal cell death in a rodent stroke model. DJ-1, a causative gene product for a familial form of Parkinson's disease, plays a role in anti-oxidative stress function by self-oxidation of DJ-1. In this study, the expression level and oxidation status of DJ-1 were examined in SHSY-5Y cells and primary cultured neurons treated with 6-hydroxydopamine (6-OHDA) or H(2)O(2) in the presence or absence of PQQ. The pI shift of DJ-1 to an acidic point, which was observed in SHSY-5Y cells treated with 6-OHDA, was inhibited by PQQ. TOF-MS analyses showed that while the level of a reduced form of DJ-1, one of the active forms of DJ-1, was decreased in SHSY-5Y cells treated with 6-OHDA or H(2)O(2), PQQ increased the level of the reduced form of DJ-1. These results suggest that PQQ prevents oxidative stress-induced changes in oxidative status of DJ-1. Therefore, the neuroprotective effects of PQQ on oxidative stress-induced neuronal death may be at least in part involved in increased level of an active form of DJ-1.The Pharmaceutical Society of Japan2008-07engjournal articleVoRhttp://hdl.handle.net/2115/53726https://doi.org/10.1248/bpb.31.1321185917680918-6158Biological & pharmaceutical bulletin31713211326https://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/53726/1/187_Ariga_2008_Biol_Pharm_Bull.pdfapplication/pdf512.0 KB2008-07